Recent theoretical and experimental work suggest that neurons need to regulate their total synaptic current and maintain an optimal activity level in order to remain responsive to continually variable input and function properly within their parent neural networks. The visual system is particularly remarkable in this regard in that it can maintain responsiveness over an enormous range of stimuli and under pathological conditions such as glaucoma where many elements of the network are damaged. How this homeostasis is maintained remains an important outstanding question. The present study is focused on a recently discovered phenomenon, Silenced Induced Potentiation (SIP), in the visual system of the goldfish. It is a large (80 percent) increase in optic synaptic efficiency that is induced by the loss of spontaneous activity in optic fibers. SIP occurs within minutes and is a strong candidate to be the first example of a rapid homeostatic response and one of the first to be seen in situ. In vivo studies on intact animals are proposed to further characterize and analyze this potentiation. These will examine its time course, longevity, localization and reversibility. Pharmacological methods will be used to analyze what transmitter systems might be responsible for regulating SIP and whether protein kinases and protein synthesis are required for its maintenance. The relationship between SIP and spontaneous postsynaptic activity will also be explored. These studies will document and analyze a new form of synaptic plasticity that may not only be important for normal function but might also underlie functional recovery following neuronal injury and disease.